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Impact of a large deletion in the neuraminidase protein identified in a laninamivir‐selected influenza A/Brisbane/10/2007 (H3N2) variant on viral fitness in vitro and in ferrets
Author(s) -
Ann Julie,
Abed Yacine,
Beaulieu Edith,
Bouhy Xavier,
Joly MarieHélène,
Dubé Karen,
Carbonneau Julie,
Hamelin MarieEve,
Mallett Corey,
Boivin Guy
Publication year - 2016
Publication title -
influenza and other respiratory viruses
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.743
H-Index - 57
eISSN - 1750-2659
pISSN - 1750-2640
DOI - 10.1111/irv.12356
Subject(s) - neuraminidase , virology , infectivity , biology , zanamivir , virus , viral replication , hemagglutinin (influenza) , in vitro , influenza a virus , medicine , covid-19 , infectious disease (medical specialty) , disease , pathology , biochemistry
Viral fitness of a laninamivir‐selected influenza A/Brisbane/10/2007‐like (H3N2) isolate (LRVp9) containing a 237‐amino acid neuraminidase deletion and a P194L hemagglutinin mutation was evaluated in vitro and in ferrets. LRVp9 and the wild‐type (WT) virus showed comparable replication kinetics in MDCK‐ST6GalI cells. Cultured virus was recovered between days 2 and 5 post‐infection in nasal washes (NW) from the 4 WT‐infected ferrets whereas no virus was recovered from the LRVp9‐infected animals. There was a ≥1 log reduction in viral RNA copies/μl of NW for LRVp9 compared to WT at most time points. The large neuraminidase deletion compromises viral infectivity in vivo .

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